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. 2020 Apr 30;295(25):8470–8479. doi: 10.1074/jbc.RA119.012365

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Figure 5. — MAP3K19 cooperates with KRAS G12C to enhance ERK activation and plays a role in maintaining cell viability in KRAS-mutant lung cancer cells. A, Western blotting analysis of MAPK phosphorylation changes because of transient expression of MAP3K19-WT, MAP3K19-KD, or KRAS G12C. The data are shown as mean protein density (phospho:total for MEK and ERK) ± S.D. B, Western blotting of endogenous MAP3K19 in lung cancer cell lines. C, top panel, RT–quantitative PCR validation of siRNA-mediated MAP3K19 knockdown in LUAD cell lines 48 h after transfection. Bottom panel, cells were seeded in 96-well plates 24 h after transfection, and cell viability was evaluated after 48 h by crystal violet assay. The data are represented as percentages of cell viability normalized to control (ctrl) ± S.D. D, phosphorylation status of MAPK family members following depletion of MAP3K19 expression in H2122 cells. The data are shown as mean phosphorylated protein density normalized to control (set to 1) ± S.D. *, p < 0.05; **, p < 0.01; ***, p < 0.001.